Search Results (5)

This study was to investigate the effects of the polysaccharides (PPM60−III) and sulfated polysaccharides (SPPM60−III) of pine pollen on the Th17/Treg balance, inflammatory cytokines, intestinal microbiota, and metabolite distribution in 3% DSS drinking water-induced UC mice. First of all, the physiological results showed that PPM60−III and SPPM60−III could alleviate UC, which was shown by the reduction in liver Treg cells, the rebalance of Th17/Treg, and the modulation of inflammatory cytokines. In addition, the 16S rRNA results showed that PPM60−III and SPPM60−III could decrease Beijerinck and Bifidobacterium, and increase Akkermansia, Escherichia coli, and Fidobacteria. Finally, the metabonomics results showed that PPM60−III and SPPM60−III also restored purine and glycerolipid metabolism, up-regulated nicotinate and nicotinamide metabolism and caffeine metabolism to inhibit inflammation. In conclusion, PPM60−III and SPPM60−III could inhibit UC by regulating gut bacteria composition and metabolite distribution; SPPM60−III showed better anti-colitis activity. Full article

Polysaccharides are important biological macromolecules in all organisms, and have recently been studied as therapeutic agents for ulcerative colitis (UC). However, the effects of Pinus yunnanensis pollen polysaccharides on ulcerative colitis remains unknown. In this study, dextran sodium sulfate (DSS) was used to induce the UC model to investigate the effects of Pinus yunnanensis pollen polysaccharides (PPM60) and sulfated polysaccharides (SPPM60) on UC. We evaluated the improvement of polysaccharides on UC by analyzing the levels of intestinal cytokines, serum metabolites and metabolic pathways, intestinal flora species diversity, and beneficial and harmful bacteria. The results show that purified PPM60 and its sulfated form SPPM60 effectively alleviated the disease progression of weight loss, colon shortening and intestinal injury in UC mice. On the intestinal immunity level, PPM60 and SPPM60 increased the levels of anti-inflammatory cytokines (IL-2, IL-10, and IL-13) and decreased the levels of proinflammatory cytokines (IL-1β, IL-6, and TNF-α). On the serum metabolism level, PPM60 and SPPM60 mainly regulated the abnormal serum metabolism of UC mice by regulating the energy-related and lipid-related metabolism pathways, respectively. On the intestinal flora level, PPM60 and SPPM60 reduced the abundance of harmful bacteria (such as Akkermansia and Aerococcus) and induced the abundance of beneficial bacteria (such as lactobacillus). In summary, this study is the first to evaluate the effects of PPM60 and SPPM60 on UC from the joint perspectives of intestinal immunity, serum metabolomics, and intestinal flora, which may provide an experimental basis for plant polysaccharides as an adjuvant clinical treatment of UC. Full article

The purpose of this study is to explore the effects of pine pollen polysaccharides and sulfated polysaccharides on mice with ulcerative colitis and whether they could protect mice from inflammation by regulating the tight junctions of colonic epithelial cells and regulating the RIPK3-dependent necroptosis pathways. Pine pollen polysaccharides were prepared by water boiling and ethanol precipitation. After deproteinedization with trichloroacetic acid, the UV spectrum showed that there were no proteins. One polysaccharide component (PPM60-III) was made by gel filtration chromatography, and then sulfated polysaccharide (SPPM60-III) was derived using the chlorosulfonic acid-pyridine method. After treatment with PPM60-III and SPPM60-III, the body weight of mice with ulcerative colitis induced by dextran sodium sulfate increased, the DAI score decreased, the levels of pro-inflammatory factors and inflammation-related enzymes decreased, and the level of anti-inflammatory factors increased. In addition, after treatment, the expressions levels of tight junction proteins increased, the expressions levels of key proteins of programmed necroptosis decreased, while the level of Caspase-8 increased. The results indicated that pine pollen polysaccharides and sulfated polysaccharides have a certain therapeutic effect on UC mice, and the therapeutic effect may be achieved by regulating the tight junction of colonic epithelial cells and regulating the RIPK3-dependent necroptosis pathways Full article

Many polysaccharides have been shown to be bioactive, with the addition of sulfate often enhancing or altering this bioactivity. In previous studies, masson pine pollen polysaccharides, to include a sulfate derivative, have been shown to promote macrophage proliferation similarly to LPS. However, the exact metabolic mechanisms promoting this proliferation remain unclear. In this study, RAW264.7 macrophage cells were treated with a purified masson pine pollen polysaccharide (PPM60-D), a sulfate derivative (SPPM60-D), or LPS. Proliferation levels at a variety of concentrations were examined using MTT assay, with optimal concentration used when performing metabolomic analysis via ¹H nuclear magnetic resonance (¹H-NMR). This process resulted in the identification of thirty-five intracellular metabolites. Subsequent multivariate statistical analysis showed that both LPS and SPPM60-D promote RAW264.7 proliferation by promoting aerobic respiration processes and reducing processes associated with glycolysis. While some insight was gained regarding the mechanistic differences between SPPM60-D and LPS, the specific mechanisms governing the effect of SPPM60 on RAW264.7 cells will require further elucidation. These findings show that both LPS and SPPM60-D effectively promote RAW264.7 proliferation and may have beneficial uses in maintaining cellular vitality or inhibiting cancer. Full article

In order to explore the immediate effect of polysaccharides and macrophages, polysaccharides from masson pine pollen (PPM60) were labeled with fluorescein isothiocyanate (FITC) by using a chemical-derived method, and the reactant was named PPM60-Tyr-FITC. Direct interaction of PPM60-Tyr-FITC and RAW264.7 macrophages could be detected by flow cytometer (FCM), and this interaction could be inhibited by Pitstop 2 (clathrin inhibitor) and TAK-242 (Toll-like receptor 4 inhibitor). The results of confocal laser scanning microscopy (CLSM) also revealed that there was a co-localization phenomenon between PPM60-Tyr-FITC and RAW264.7 macrophage receptors, and it could be suppressed by Pitstop 2 and TAK-242. It was confirmed that PPM60 enters into RAW264.7 macrophages mainly through endocytosis, rather than the phagocytosis, and TLR4 played a mediating role. Full article